Anatomy of Declarative Memory

A broad convergence of human and animal research indicates that declarative memory depends on an interaction between domain-specific neocortical regions and domain-independent medial-temporal, diencephalic, and basal forebrain regions. ^ Long-term memories are thought to be stored in the neocortex, the neocortical location reflecting the content of the memory. Thus, knowledge about the visual appearance of a tool may be stored separately,



Anatomic Site of Damage

Memory Finding

Other Neurological and Medical Findings

Frontal lobe

Lateralized deficits in working memory. Right spatial defects, left verbal defects, impaired recall with spared recognition

Personality change Perseveration Chorea, dystonia Bradykinesia, tremor, rigidity

Basal forebrain

Domain-independent declarative memory deficits

Ventromedial cortex

Frontal lobe-type declarative memory deficits

Upper visual field defects

Hippocampus and parahippocampal cortex

Bilateral lesions yield global amnesia, unilateral lesions show lateralization of deficits--left: verbal deficits; right: spatial deficits


Depressed level of consciousness Cortical blindness Autonomations


Global amnesia

Mammillary bodies

Declarative memory deficits

Confabulation, ataxia, nystagmus, signs of alcohol withdrawal

Dorsal and medial dorsal nucleus thalamus

Declarative memory deficits


Anterior thalamus

Declarative memory deficits

Lateral temporal cortex

Deficits in autobiographical memory

Figure 5-1 (Figure Not Available) Papez circuit that integrates cortical and subcortical structures involved in memory or emo(From Goetz CG, Wilson RS: Behavioral Neurology. In Weiner WJ and Goetz CG [eds]: Neurology for the Non-Neurologist. Philadelphia, J.B. Lippincott, 1994, pp 184-194.)

perhaps near the visual neocortex, from knowledge about its use, which may be stored in areas that include the premotor areas. [8] Memory of an event or fact, therefore, may be widely distributed in the neocortex with specific perceptual, conceptual, and emotional features of an event stored in specialized neocortical regions. The hippocampal complex has reciprocal connections with higher-order association cortices, and it is hypothesized that the hippocampal complex somehow binds or relates multiple features about an event or fact across physically disparate neocortical regions. Over time, the features somehow become consolidated and no longer require the hippocampal complex for binding. It is thought that temporally limited retrograde amnesia reflects the disruption of consolidation processes.

Damage to a neocortical region results in both the loss of previously acquired memory, or knowledge, stored in that area and an inability to acquire new memories involving that kind of knowledge. For example, patients with left temporal lesions lose specific knowledge about the names of animals, tools, or people, depending on the location of the lesion.y Thus, neocortical damage is thought to result in domain-specific memory deficits in which the loss of old memories and the inability to gain new memories reflect the kind of knowledge represented in that neocortical region.

In contrast, damage to medial temporal lobe, diencephalic, and basal forebrain regions yield widespread, or domain-independent, declarative memory deficits. Global amnesia can arise from damage to any one of these regions, even if the other regions remain intact. Bilateral damage to these regions can yield a global amnesia that affects all domains of declarative memory. Unilateral left- or right-sided lesions typically result in material-specific memory dysfunctions for, respectively, verbal or nonverbal information. An important exception to this rule occurs in patients with longstanding unilateral injury, such as that seen sometimes in epilepsy. In such cases, the relatively spared contralateral brain region may become critical for verbal and nonverbal memory functions.

The medial-temporal region includes a number of interconnected but anatomically distinct structures: the amygdala, the hippocampal region that includes the cornu ammonis (CA) fields, dentate gyrus, and subiculum; the entorhinal cortex; the perirhinal cortex; and the parahippocampal cortex. Research with animals and humans indicates that these structures all have their own specialized roles in memory. It is now thought that the amygdala is not critical for most aspects of declarative memory. Rather, the amygdala appears to play a specific role in the emotional modulation of memories; its role in fear conditioning is especially well documented. y Focal damage to the CA1 region of the hippocampus is sufficient to result in a clinically substantial declarative memory deficit. y More widespread damage to the entorhinal, perirhinal, and parahippocampal regions results in increasingly devastating memory deficits. y In addition, the fornix constitutes the major subcortical output pathway of the hippocampal region. Damage to the fornix can produce global amnesia. y The specific mnemonic roles of medial temporal lobe regions critical for declarative memory ability have not yet been characterized in humans.

Diencephalic regions linked to declarative memory include the dorsomedial and anterior nuclei of the thalamus, the mammillary bodies, the mammillothalamic fiber tract connecting the medial hippocampal complex to the anterior thalamic nuclei, and the ventroamygdalofugal fiber tract connecting the amygdala to the dorsomedial nuclei. The precise roles of these structures are not well specified, in part because damage tends to co-occur in multiple structures. For example, the mammillary bodies and dorsomedial nuclei are both greatly affected in alcoholic Korsakoff's amnesia. Acute thalamic lesions producing amnesia often injure both the dorsomedial nucleus and the surrounding mammillothalamic and ventroamygdalofugal tracts. The preponderance of the evidence favors a critical role for the dorsomedial nucleus of the thalamus and, perhaps, the surrounding fibers of the mammillothalamic tract. y The importance of the mammillary bodies is less certain. Lesions there sometimes appear to account for declarative memory deficits in patientsy but do not produce the long-lasting memory impairments seen in monkeys that have sustained medial-temporal or dorsomedial thalamic lesions. Declarative memory failure after diencephalic lesions appears to be quite similar to that seen after medial-temporal lesions, although additional nonmnemonic deficits may result from diencephalic lesions. The basal forebrain is composed of midline structures

including the septal nuclei, diagonal band of Broca, and substantia innominata. These regions provide the largest input of acetylcholine, the neurotransmitter most directly implicated as critical for declarative memory, to the hippocampus and many neocortical areas. The basal forebrain also supplies to the cerebral cortex other neurotransmitters that contribute to the modulation of memory, including dopamine, norepinephrine, and serotonin. An extensive lesion to the basal forebrain yields a severe declarative memory impairment.'^ Partial damage to this and adjacent ventromedial frontal cortex often occurs after ruptures of anterior communicating artery aneurysms, which often lead to mild but persistent anterograde amnesia. y

There is increasing evidence of a correlation between the severity of anterograde amnesia and the extent of retrograde amnesia. Further, the severity of both anterograde and retrograde amnesia appear to correlate with the extent of medial-temporal injury. [ii] Some patients with mild anterograde amnesias, however, show a surprising loss of personal memories concerning major life events or family members. y These patients typically have sustained damage to the more lateral temporal neocortex, which may store long-term autobiographical memory representations. These patients fail to exhibit the temporally graded retrograde amnesia characteristic of patients with lesions restricted to medial-temporal areas.

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